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Ann Thorac Surg 1996;62:796-797
© 1996 The Society of Thoracic Surgeons
DR WALTER KLEPETKO (Vienna, Austria): Doctor Yamashita, I congratulate you on this well-designed, timely, and interesting study.
Nitric oxide has played an important role within the last years. Although its mechanism of acting is by far not completely understood, it has a tremendous potential and striking effects on pulmonary circulation and gas exchange as well. This has led to a widespread application of its inhaled form for treatment of patients with different forms of pulmonary insufficiency. The effects of nitroprusside administration you have shown us are striking as well, and improvement in oxygenation is far more impressive than has been demonstrated for almost any other substance that has been investigated in the field of lung transplantation.
I have a couple of questions addressing the use of intravenous nitroprusside in comparison with inhaled nitric oxide. First, how long does it take until nitroprusside administration results in effective increase of nitric oxide? Second, from the use of inhaled nitric oxide, we know that its effect is immediately reversible with the end of its administration. Are there data that demonstrate that the same holds true for the intravenous application of nitroprusside? And third, can you tell us what the advantage of nitroprusside is compared with other potential nitric oxide donors?
To sum it up, among the different substances that have been investigated in lung preservation, I think nitroprusside is one that really has the potential to make its way into clinical practice.
DR YAMASHITA: Thank you for the questions.
With regard to the second question, nitroprusside has a strong vasodilatory effect, so when comparing it with the other kinds of nitric oxide donors, like nitroglycerin, it is sometimes difficult to maintain systemic vascular resistance. In these experiments I adjusted the continuous dose to 0.1 mg/kg. This was associated with a significant decrease in blood pressure. Furthermore, nitroprusside releases nitric oxide directly after reacting with the plasma, but in the case of nitroglycerin it takes a little bit longer. So I think when we use nitroprusside in a flush solution or just around the time of the reperfusion, it is better than nitroglycerin.
DR KLEPETKO: How long does the effect of nitroprusside administration last? If you take nitroprusside infusion away from the animals during the experiment (and I do not know whether you have investigated that), is the beneficial effect still there over the next period of time or do you see immediately decreasing lung function, like we have seen in patients with nitric oxide inhalation?
DR PATTERSON: We do not know the answer to that question. I would expect that it would not be such an immediate effect because I think nitroprusside has other actions as well, but we did not study this effect in this particular model.
DR THOMAS M. EGAN (Chapel Hill, NC): It is the other actions of nitroprusside that I am curious about. How do you know that what you are seeing is due to nitric oxide? Could it be that it is because of a vasodilator that is distributing blood flow to the lung differently?
DR YAMASHITA: Yes, it is true. Judging from these experimental studies, I cannot separate the vasodilative effect and the nitric oxide donor effect, so it is hard to answer Dr Egan's question.
DR THOMAS R. J. TODD (Toronto, Ont, Canada): I would just like to expand upon Dr Egan's question. Your report is an excellent one and intrigues me more than it answers questions for me. We know historically that nitroprusside can profoundly improve ventilation-perfusion mismatching in many different situations of lung injury. As shown by your data, the principal thing that you did was improve cardiac output. There is no real change in pulmonary artery pressure that I can see, so your change in pulmonary vascular resistance is a calculated change in pulmonary vascular resistance. Therefore Dr Egan's question, I think, is very germane. Specifically, did you obtain any measurements of acid-base balance or any peripheral mediators that might have been generated during the perfusion that might have had an adverse effect or ameliorative effect on your lung functions because of an improvement in peripheral circulation?
DR PATTERSON: You are right; I agree that the change in pulmonary vascular resistance here is cardiac output. I do not know why the cardiac output was higher in the nitroprusside group. Maybe the oxygenation was so terrible in the control group that it decreased cardiac output. I think that is the mechanism of that particular hemodynamic observation. We did not measure any peripheral assays. We did not make any observations at all that might specifically address the nitric oxide generation, like nitrate/nitrite ratios. But there is no question that there are very few drugs that produce the profound depression of neutrophil sequestration that we observed. That is a significant observation, and I do not think that it is due to a hemodynamic effect of nitroprusside.
Related Article
Ann. Thorac. Surg. 1996 62: 791-796.
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